The impact of ischemic preconditioning (IPC) on contraction, Ca²⁺ homeostasis and cell survival was compared in isolated ventricular myocytes from young adult (~3 mos) and aged (~24 mos) male Fischer 344 rats. Myocytes were field-stimulated at 4 Hz (37°C). Contraction (edge detector) and intracellular Ca²⁺ (fura-2) were measured simultaneously. Cell viability was assessed with Trypan blue. All cells were exposed to 30 mins of simulated ischemia followed by reperfusion. Some cells were preconditioned by exposure to 5 mins of simulated ischemia prior to prolonged ischemia. Pre-treatment with IPC abolished stunning, inhibited diastolic contracture and increased Ca²⁺ transient amplitudes in reperfusion in young adult and aged cells. IPC did not affect the modest rise in diastolic Ca²⁺ in ischemia in young adult myocytes. However, IPC abolished the marked rise in diastolic Ca²⁺ observed in ischemia and early reperfusion in aged myocytes. IPC also suppressed mechanical alternans in ischemia in aged cells, but younger myocytes showed little evidence of mechanical alternans, whether or not cells were preconditioned. IPC markedly improved cell viability in reperfusion in younger cells, but not in aged cells. These results suggest that IPC augments recovery of contractile function in reperfusion by increasing Ca²⁺ transient amplitudes in ventricular myocytes from young adult and aged rats. IPC reduced diastolic Ca²⁺ accumulation in ischemia in aged myocytes, which may diminish the severity of mechanical alternans in aged cells. Nonetheless, the efficacy of IPC is compromised in aging, as IPC did not improve survival of aged myocytes exposed to ischemia and reperfusion.